scholarly journals Night-shift work is associated with poorer glycaemic control in patients with type 2 diabetes

2017 ◽  
Vol 26 (6) ◽  
pp. 764-772 ◽  
Author(s):  
Areesa Manodpitipong ◽  
Sunee Saetung ◽  
Hataikarn Nimitphong ◽  
Nantaporn Siwasaranond ◽  
Thanawat Wongphan ◽  
...  
Diabetes Care ◽  
2018 ◽  
Vol 41 (4) ◽  
pp. 762-769 ◽  
Author(s):  
Céline Vetter ◽  
Hassan S. Dashti ◽  
Jacqueline M. Lane ◽  
Simon G. Anderson ◽  
Eva S. Schernhammer ◽  
...  

BMJ ◽  
2018 ◽  
pp. k4641 ◽  
Author(s):  
Zhilei Shan ◽  
Yanping Li ◽  
Geng Zong ◽  
Yanjun Guo ◽  
Jun Li ◽  
...  

AbstractObjectivesTo prospectively evaluate the joint association of duration of rotating night shift work and lifestyle factors with risk of type 2 diabetes risk, and to quantitatively decompose this joint association to rotating night shift work only, to lifestyle only, and to their interaction.DesignProspective cohort study.SettingNurses’ Health Study (1988-2012) and Nurses’ Health Study II (1991-2013).Participants143 410 women without type 2 diabetes, cardiovascular disease, or cancer at baseline.ExposuresRotating night shift work was defined as at least three night shifts per month in addition to day and evening shifts in that month. Unhealthy lifestyles included current smoking, physical activity levels below 30 minutes per day at moderate to vigorous intensity, diet in the bottom three fifths of the Alternate Healthy Eating Index score, and body mass index of 25 or above.Main outcome measuresIncident cases of type 2 diabetes were identified through self report and validated by a supplementary questionnaire.ResultsDuring 22-24 years of follow-up, 10 915 cases of incident type 2 diabetes occurred. The multivariable adjusted hazard ratios for type 2 diabetes were 1.31 (95% confidence interval 1.19 to 1.44) per five year increment of duration of rotating night shift work and 2.30 (1.88 to 2.83) per unhealthy lifestyle factor (ever smoking, low diet quality, low physical activity, and overweight or obesity). For the joint association of per five year increment rotating night shift work and per unhealthy lifestyle factor with type 2 diabetes, the hazard ratio was 2.83 (2.15 to 3.73) with a significant additive interaction (P for interaction <0.001). The proportions of the joint association were 17.1% (14.0% to 20.8%) for rotating night shift work alone, 71.2% (66.9% to 75.8%) for unhealthy lifestyle alone, and 11.3% (7.3% to 17.3%) for their additive interaction.ConclusionsAmong female nurses, both rotating night shift work and unhealthy lifestyle were associated with a higher risk of type 2 diabetes. The excess risk of rotating night shift work combined with unhealthy lifestyle was higher than the addition of risk associated with each individual factor. These findings suggest that most cases of type 2 diabetes could be prevented by adhering to a healthy lifestyle, and the benefits could be greater in rotating night shift workers.


2012 ◽  
Vol 17 (6) ◽  
pp. 193-194 ◽  
Author(s):  
John Axelsson ◽  
Sampsa Puttonen

2021 ◽  
pp. 30-33
Author(s):  
David Jaynes ◽  
Paul Switzer

The purpose of this article is to provide background information and the current understanding of a less familiar cause of female breast cancer; exposure to ultraviolet light at night. Breast cancer is a common disease that causes significant morbidity and mortality in women. There are several risk factors for breast cancer, most of which are genetic and environmental in nature. An often-overlooked risk factor is exposure to blue light during night shift work, which decreases melatonin production. One of the many cancer-preventing properties of melatonin is to limit estrogen production. Increased lifetime exposure to estrogen is a well-known cause of breast cancer. Awareness of nighttime blue light exposure as a breast cancer risk factor by women doing night shift work and those exposed to nighttime light via smartphones and laptops, is essential information to know so that protective measures can be taken.


2013 ◽  
Vol 3 (1) ◽  
pp. 11-18 ◽  
Author(s):  
Zafar Ahmed Latif ◽  
Md. Faruque Pathan ◽  
Md. Nazrul Islam Siddiqui ◽  
MA Mannan ◽  
SM Ashrafuzzaman ◽  
...  

Objective: To present results from the Bangladesh cohort of the A1chieve study receiving insulin detemir (Levemir) ± oral anti diabetic drugs. Methods: Out of 1093 patients recruited from 49 sites in Bangladesh, 370 were initiated on insulin detemir (Levemir).Study visits were defined as baseline, interim (around 12 weeks from baseline) and final (around 24 weeks from baseline) visit. Results: Glycaemic control was poor in all the groups at baseline. In the entire cohort at 24 weeks, significant reductions from baseline were observed in mean HbA1c (from 10.0 % to 7.2%, p<0.001), FPG (from 10.5 to 6.7 mmol/L, p<0.001) and PPPG (from 15.3 to 8.9 mmol/L, p<0.001) levels. Overall 45.5% of the participants achieved target HbA1c level of < 7% after 24 weeks. The rate of all hypoglycaemic events in the entire cohort reduced from 1.34 (baseline) to 0.12 events/person year after 24 weeks of insulin detemir therapy (p<0.0001). There was no clinically relevant change in body weight in insulin naïve or prior insulin users groups after 24 weeks of insulin detemir therapy. Conclusions: The current study suggests that insulin detemir may be considered as a safe and effective option for initiating insulin therapy for type 2 diabetes in Bangladesh. Birdem Med J 2013; 3(1): 11-18 DOI: http://dx.doi.org/10.3329/birdem.v3i1.17121


2011 ◽  
pp. 5-10
Author(s):  
Huu Dang Tran

The incretins are peptide hormones secreted from the gut in response to food. They increase the secretion of insulin. The incretin response is reduced in patients with type 2 diabetes so drugs acting on incretins may improve glycaemic control. Incretins are metabolised by dipeptidyl peptidase, so selectively inhibiting this enzyme increases the concentration of circulating incretins. A similar effect results from giving an incretin analogue that cannot be cleaved by dipeptidyl peptidase. Studies have identified other actions including improvement in pancreatic β cell glucose sensitivity and, in animal studies, promotion of pancreatic β cell proliferation and reduction in β cell apoptosis.


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